MicroRNA-7 deficiency ameliorates d-galactose-induced aging in mice by regulating senescence of Kupffer cells
© 2024 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd..
Aging is intricately linked to immune system dysfunction. Recent studies have highlighted the biological function of microRNA-7 (miR-7) as a novel regulator of immune cell function and related diseases. However, the potential role of miR-7 in aging remains unexplored. Here, we investigated the contribution of miR-7 to d-gal-induced aging in mice, focusing on its regulation of senescent Kupffer cells. Our findings revealed that miR-7 deficiency significantly ameliorated the aging process, characterized by enhanced CD4+ T-cell activation. However, the adoptive transfer of miR-7-deficient CD4+ T cells failed to improve the age-related phenotype. Further analysis showed that miR-7 deficiency significantly reduced IL-1β production in liver tissue, and inhibiting IL-1β in vivo slowed down the aging process in mice. Notably, IL-1β is mainly produced by senescent Kupffer cells in the liver tissue of aging mice, and miR-7 expression was significantly up-regulated in these cells. Mechanistically, KLF4, a target of miR-7, was down-regulated in senescent Kupffer cells in aging mouse model. Furthermore, miR-7 deficiency also modulated the NF-κB activation and IL-1β production in senescent Kupffer cells through KLF4. In conclusion, our findings unveil the role of miR-7 in d-gal-induced aging in mice, highlighting its regulation of KLF4/NF-κB/IL-1β pathways in senescent Kupffer cells. This research may enhance our understanding of miRNA-based aging immune cells and offer new avenues for new intervention strategies in aging process.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - year:2024 |
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| Enthalten in: |
Aging cell - (2024) vom: 17. März, Seite e14145 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Ya [VerfasserIn] |
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| Links: |
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| Themen: |
Aging |
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| Anmerkungen: |
Date Revised 18.03.2024 published: Print-Electronic Citation Status Publisher |
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| doi: |
10.1111/acel.14145 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM369843460 |
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| 520 | |a © 2024 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd. | ||
| 520 | |a Aging is intricately linked to immune system dysfunction. Recent studies have highlighted the biological function of microRNA-7 (miR-7) as a novel regulator of immune cell function and related diseases. However, the potential role of miR-7 in aging remains unexplored. Here, we investigated the contribution of miR-7 to d-gal-induced aging in mice, focusing on its regulation of senescent Kupffer cells. Our findings revealed that miR-7 deficiency significantly ameliorated the aging process, characterized by enhanced CD4+ T-cell activation. However, the adoptive transfer of miR-7-deficient CD4+ T cells failed to improve the age-related phenotype. Further analysis showed that miR-7 deficiency significantly reduced IL-1β production in liver tissue, and inhibiting IL-1β in vivo slowed down the aging process in mice. Notably, IL-1β is mainly produced by senescent Kupffer cells in the liver tissue of aging mice, and miR-7 expression was significantly up-regulated in these cells. Mechanistically, KLF4, a target of miR-7, was down-regulated in senescent Kupffer cells in aging mouse model. Furthermore, miR-7 deficiency also modulated the NF-κB activation and IL-1β production in senescent Kupffer cells through KLF4. In conclusion, our findings unveil the role of miR-7 in d-gal-induced aging in mice, highlighting its regulation of KLF4/NF-κB/IL-1β pathways in senescent Kupffer cells. This research may enhance our understanding of miRNA-based aging immune cells and offer new avenues for new intervention strategies in aging process | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a IL-1β | |
| 650 | 4 | |a KLF4 | |
| 650 | 4 | |a aging | |
| 650 | 4 | |a microRNA-7 | |
| 650 | 4 | |a senescent Kupffer cells | |
| 700 | 1 | |a Qiu, Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Shipeng |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Dongmei |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Xu |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Mengmeng |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Nana |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Chao |e verfasserin |4 aut | |
| 700 | 1 | |a Qin, Ming |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Ya |e verfasserin |4 aut | |
| 700 | 1 | |a Xiao, Daimin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Juanjuan |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Lin |e verfasserin |4 aut | |
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